Role of peroxisome proliferators activated receptor gamma in mediating proliferation of rat vascular smooth muscle cells induced by advanced glycation end products.
- Author:
Xiao-chen YUAN
1
;
Nai-feng LIU
;
Jin-chuan YAN
;
Xin ZHANG
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Cell Proliferation; drug effects; Cells, Cultured; Glycation End Products, Advanced; metabolism; pharmacology; Muscle, Smooth, Vascular; cytology; Myocytes, Smooth Muscle; cytology; PPAR gamma; metabolism; pharmacology; Rats; Rats, Sprague-Dawley; Thiazolidinediones; pharmacology
- From: Chinese Journal of Cardiology 2005;33(10):940-944
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo observe the effect of pioglitazone on advanced glycation end products (AGEs)-induced proliferation of vascular smooth muscle cells (VSMCs) and expression of peroxisome proliferators activated receptor gamma (PPARgamma). To investigate the possible role of PPARgamma in mediating AGEs induced proliferation of VSMCs.
METHODSPrimary cultures of smooth muscle cells from rat aorta were exposed to AGEs of different concentrations and different times prior to co-treatment with pioglitazone and AGEs. 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyl tetrazolium bromide (MTT) assay was adopted for the quantification of the cell proliferation ratio and PPARgamma expression was determined by RT-PCR and Western immunoblotting.
RESULTSAGEs increased the proliferation of VSMCs. AGEs treatment to VSMCs decreased mRNA and protein levels of PPARgamma in a time- and dose-related manner (P < 0.05). Pioglitazone inhibited the AGEs-induced proliferation of VSMCs in vitro.
CONCLUSIONSActivating PPARgamma in VSMCs, pioglitazone may play a role in anti atherosclerosis. The reduction in PPARgamma expression may be implicated in vascular smooth muscle cells proliferation and pathogenesis of atherosclerosis in patients with diabetes mellitus.
